The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index; 1 of the 19 sources its claims cite were checked for support.
Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program
Open accessAbstract
Insulin resistance and beta-cell dysfunction, two factors central to the pathogenesis of type 2 diabetes, were studied in relation to the development of diabetes in a group of participants with impaired glucose tolerance in the Diabetes Prevention Program (DPP) at baseline and after specific interventions designed to prevent diabetes. Participants were randomly assigned to placebo (n = 1,082), metformin (850 mg twice a day) (n = 1,073), or intensive lifestyle intervention (n = 1,079). The diabetes hazard rate was negatively associated with baseline insulin sensitivity (hazard rate ratio = 0.62-0.94 per SD difference, depending on treatment group and measure of sensitivity) and with baseline insulin secretion (hazard rate ratio = 0.57-0.76 per SD). Improvements in insulin secretion and insulin sensitivity were associated with lower hazard rates in all treatment arms (hazard rate ratio = 0.46-0.95 per SD increase and 0.29-0.79 per SD increase, respectively). In multivariate models that included the three metabolic variables (changes in body weight, insulin sensitivity, and insulin secretion) each significantly and independently predicted progression to diabetes when adjusted for the other two variables. The intensive lifestyle intervention, which elicited the greatest reduction in diabetes incidence, produced the greatest improvement in insulin sensitivity and the best preservation of beta-cell function after 1 year, whereas the placebo group, which had the highest diabetes incidence, had no significant change in insulin sensitivity and beta-cell function after 1 year. In the metformin group, diabetes risk, insulin sensitivity, and beta-cell function at 1 year were intermediate between those in the intensive lifestyle and placebo groups. In conclusion, higher insulin secretion and sensitivity at baseline and improvements in response to treatment were associated with lower diabetes risk in the DPP. The better preventive effectiveness of intensive lifestyle may be due to improved insulin sensitivity concomitant with preservation of beta-cell function.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
59 Own result · 15 Own interpretation · 10 No full text of the sources · 4 No basis given · 2 Own method · 1 Partly supported · 1 Sources not found · 1 Not checked yet · accuracy not yet measured
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Correlations between the year 1 changes in metabolic variables were similar among the treatment groups, except for the correlations between 1/fasting insulin and either CIR or IGR, which were higher in the metformin group.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in metabolic variables over time.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Improvements in insulin secretion and insulin sensitivity were associated with lower hazard rates in all treatment arms (hazard rate ratio ؍ 0.46 -0.95 per SD increase and 0.29 -0.79 per SD increase, respectively).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Hazard ratios were constant over time.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The hazard rates for developing diabetes were positively associated with baseline fasting plasma glucose, 120-min plasma glucose, and A1C (Fig. 3).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Prediction of diabetes by individual metabolic factors
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Hazard ratios were constant over time.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In this large cohort of individuals with IGT, our results clearly confirm this relationship because each variable had an independent effect on the risk of developing diabetes.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Fasting and 30-and 120-min glucose values decreased significantly in the lifestyle group”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in metabolic variables over time.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
The paper states this without a source or data behind it here, so there is nothing to check it against. The quote shows it is in the paper.
In the paper
“this change was relatively less than the change in insulin sensitivity”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“whereas the placebo group, which had the highest diabetes incidence, had no significant change in insulin sensitivity and -cell function after 1 year.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Abstract
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“and with baseline insulin secretion (hazard rate ratio ؍ 0.57-0.76per SD).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Abstract
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Hazard ratios were constant over time.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the lifestyle and placebo groups, hazard rates were negatively associated with baseline 1/fasting insulin.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Baseline and changes in body weight, insulin sensitivity, and insulin secretion.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Hazard ratios were constant over time.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The hazard rates for diabetes were positively associated with baseline weight in the lifestyle and placebo groups when adjusted for baseline demographics (age, sex, and race/ethnicity) (Fig. 4, left panels).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Baseline and changes in body weight, insulin sensitivity, and insulin secretion.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
- The authors state this as an assumption: Hazard ratios were constant over time.
- It may state two separate claims as one. 24
- Probably not a substantial claim. 7
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The latter two are strong risk factors for type 2 diabetes (1-6).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Abstract
What the sources say
- Not checked — no full text of the sourcecites [1] The Diabetes Prevention Program Research Group: Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 346:393–403,2002 source
- Partly supportedcites [2] Modan M, Karasik A, Halkin H, Fuchs Z, Lusky A, Shitrit A, Modan B: Effect of past and concurrent body mass index on prevalence of glucose intolerance and type 2 (non-insulin-dependent) diabetes and on insulin response: the Israel study of glucose intolerance, obesity and hypertension. Diabetologia 29:82–89,1986 sourceExperimental — accuracy not yet measured
The BMI INTERVAL section describes impaired glucose tolerance progressing to Type 2 diabetes, and the Discussion likewise describes worsening from impaired tolerance to diabetes. But the paper does not address impaired fasting glycemia or establish that both conditions are strong risk factors. Page numbers are unavailable in our copy. (LLM, conf=0.84)
- Not checked — no full text of the sourcecites [3] Saad MF, Knowler WC, Pettitt DJ, Nelson RG, Mott DM, Bennett PH: The natural history of impaired glucose tolerance in the Pima Indians. N Engl J Med 319:1500–1506,1988 source
- Not checked — no full text of the sourcecites [4] Lillioja S, Mott DM, Howard BV, Bennett PH, Yki-Jarvinen H, Freymond D, Nyomba BL, Zurlo F, Swinburn B, Bogardus C: Impaired glucose tolerance as a disorder of insulin action: longitudinal and cross-sectional studies in Pima Indians. N Engl J Med 318:1217–1225,1988 source
- Not checked — no full text of the sourcecites [5] Edelstein SL, Knowler WC, Bain RP, Andres R, Barrett-Connor EL, Dowse GK, Haffner SM, Pettitt DJ, Sorkin JD, Muller DC, Collins VR, Hamman RF: Predictors of progression from impaired glucose tolerance to NIDDM: an analysis of six prospective studies. Diabetes 46:701–710,1997 source
- Not checked — no full text of the sourcecites [6] Jensen CC, Cnop M, Hull RL, Fujimoto WY, Kahn SE, American Diabetes Association GENNID Study Group: β-Cell function is the major determinant of oral glucose tolerance in four ethnic groups in the United States. Diabetes 51:2170–2178,2002 source
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“At 1 year, there was less reduction in fasting insulin in the metformin than in the lifestyle group, with the lifestyle participants having the greatest reduction throughout all years of follow-up.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in metabolic variables over time.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“ISI and 1/fasting insulin were, as expected, highly correlated at baseline (Spearman r ϭ 0.99).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > July 2001 (see DATA ANALYSIS).
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Encompassing of the additional follow-up data yielded risk reductions (95% CI) of developing diabetes of 30% (16 -41%) for metformin and 55% (45-63%) for lifestyle, each compared with placebo.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > July 2001 (see DATA ANALYSIS).
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, we found that A1C, proinsulin, insulin sensitivity, and insulin secretion also predicted the development of diabetes in these high-risk individuals.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Among all participants, including those who developed diabetes, fasting glucose, insulin, and proinsulin concentrations were significantly lower than placebo at the first annual visit in the metformin and the lifestyle groups and increased during the 2nd and 3rd years, with the levels remaining significantly lower than in the placebo group (Fig. 2).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in metabolic variables over time.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In the placebo group, however, there was a significant increase in 30-min and a significant decrease in the 120-min glucose levels.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in metabolic variables over time.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: unclear — It is unclear whether the paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Whereas lifestyle and metformin treatments reduced the incidence of diabetes, they did not change the independent effects of insulin sensitivity and secretion on the risk for diabetes, so that those individuals with the lowest sensitivity and secretion within each treatment group still had the greatest risk, whereas those with the highest insulin sensitivity and secretion had uniformly low risk”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Changes in weight and proinsulin over time were strong predictors of diabetes, with decreased weight and decreased proinsulin predicting a lower hazard of diabetes in all treatment arms (Fig. 4B and D).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Baseline and changes in body weight, insulin sensitivity, and insulin secretion.
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- The authors state this as an assumption: Hazard ratios were constant over time.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The metformin group showed a more modest improvement in insulin sensitivity (ISI and 1/fasting insulin, P Ͻ 0.001) with a significant decrease in insulin secretion (IGR, P Ͻ 0.001)”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in insulin secretion and sensitivity.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In addition, improved insulin sensitivity was also associated with a decrease in the risk of developing diabetes, with the lifestyle intervention again being the most effective.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Finally, in the placebo group there were no significant changes in either estimate of insulin sensitivity, a significant decrease in insulin secretion (IGR, P ϭ 0.03) but no significant change in -cell function”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in insulin secretion and sensitivity.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The intensive lifestyle intervention, which elicited the greatest reduction in diabetes incidence, produced the greatest improvement in insulin sensitivity and the best preservation of -cell function after 1 year”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Abstract
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The lifestyle group had the greatest improvement in insulin sensitivity (ISI and 1/fasting insulin, P Ͻ 0.001), and this was associated with a significant decrease in insulin secretion (IGR, P ϭ 0.008).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in insulin secretion and sensitivity.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The relationships in the current data were not hyperbolic but were well described as nonlinear.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
boostedcorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The risk of developing diabetes was lowest among participants in the lifestyle arm, intermediate among those assigned to metformin, and highest among placebo participants across the range of baseline glycemic variables.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Prediction of diabetes by individual metabolic factors
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In general, these treatment effects were seen regardless of the categories of sensitivity and secretion, except in the lowest risk categories (high insulin sensitivity and secretion), in which hazard rates were uniformly low.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Prediction of diabetes by multiple metabolic factors Baseline insulin sensitivity and insulin secretion.
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“found that the risk for developing type 2 diabetes was reduced by 58 and 31% in the intensive lifestyle and metformin-treated groups, respectively, compared with the placebo-treated group (1).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Abstract
What the sources say
- Not checked — no full text of the sourcecites [1] The Diabetes Prevention Program Research Group: Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 346:393–403,2002 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“These findings are compatible, with lifestyle having the greatest effect to preserve -cell function and it being the more effective intervention to reduce the rate of development of diabetes.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
hedgeddirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The three scenarios (no change, improvement, decrease in β-cell function) exhaustively characterize possible changes in the insulin secretion-sensitivity relationship.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Finally, a decrease in -cell function would be characterized by a shift to the left of or below the curve.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus, it would appear that -cell function was unchanged in the lifestyle intervention group while declining in the control group.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
hedged- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The three scenarios (no change, improvement, decrease in β-cell function) exhaustively characterize possible changes in the insulin secretion-sensitivity relationship.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Ninety-five percent of participants completed their first annual visit.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Table 1 presents baseline characteristics by treatment group.
plain- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
In the paper
“This hyperbolic relationship has previously been described when more direct measures of insulin secretion and sensitivity were used (29).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
What the sources say
- Not checked — no full text of the sourcecites [29] Kahn SE, Prigeon RL, McCulloch DK, Boyko EJ, Bergman RN, Schwartz MW, Neifing JL, Ward WK, Beard JC, Palmer JP, Porte D Jr: Quantification of the relationship between insulin sensitivity and B-cell function in human subjects: evidence for a hyperbolic function. Diabetes 42:1663–1672,1993 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Lifestyle intervention and, to a lesser extent, metformin enhanced -cell function and improved insulin sensitivity, leading to a reduced risk for developing diabetes.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The baseline relationship between insulin secretion and insulin sensitivity is the same across treatment groups.
- Rests on an assumption: The three scenarios (no change, improvement, decrease in β-cell function) exhaustively characterize possible changes in the insulin secretion-sensitivity relationship.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Thus it appears that whereas change in body weight was a strong predictor of the risk of developing diabetes in the DPP, the interventions probably had differential effects on other variables or direct effects in the liver or muscle even after accounting for insulin secretion.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
hedgedconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
In the paper
“Similar findings of the effect of lifestyle intervention have been reported for the Finnish Diabetes Prevention Study (30).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
What the sources say
- Not checked — no full text of the sourcecites [30] Uusitupa M, Lindi V, Louheranta A, Salopuro T, Lindström J, Tuomilehto J, Finnish Diabetes Prevention Study Group: Long-term improvement in insulin sensitivity by changing lifestyles of people with impaired glucose tolerance: 4-year results from the Finnish Diabetes Prevention Study. Diabetes 52:2532–2538,2003 source
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“but whereas the absolute response declined, this decrease was not as large as might be expected from the concomitant change in insulin sensitivity and therefore can be interpreted as improved secretion relative to sensitivity.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > Changes in insulin secretion and sensitivity.
plaincorrelational- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
A claim is checked only against the cited paper’s full text, never its abstract, and none is available for its sources.
In the paper
“this process is never complete so that not all proinsulin molecules are cleaved, resulting in a small quantity of proinsulin being secreted along with insulin and C-peptide (36 -38).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
What the sources say
- Not checked — no full text of the sourcecites [36] Kitabchi AE: Proinsulin and C-peptide a review. Metabolism 26:547–587,1977 source
- Not checked — no full text of the sourcecites [37] Mykkanen L, Haffner SM, Hales CN, Ronnemaa T, Laakso M: The relation of proinsulin, insulin, and proinsulin-to-insulin ratio to insulin sensitivity and acute insulin response in normoglycemic subjects. Diabetes 46:1990–1995,1997 source
- Not checked — no full text of the sourcecites [38] Reaven GM, Chen Y-DI, Hollenbeck CB, Sheu WHH, Ostrega D, Polonsky KS: Plasma insulin, C-peptide, and proinsulin concentrations in obese and nonobese individuals with varying degrees of glucose tolerance. J Clin Endocrinol Metab 76:44–48,1993 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The effect of metformin and intensive lifestyle in reducing the incidence of diabetes is related in part to their ability to shift the relationship between insulin sensitivity and insulin secretion in a direction compatible with an improvement in -cell function, with lifestyle being more effective in doing so.”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
plainconditional- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: passes — The paper’s conclusions depend on it.
- Based: passes — The paper gives a reason why it holds.
It may state two separate claims as one.
- Rests on an assumption: The baseline relationship between insulin secretion and insulin sensitivity is the same across treatment groups.
- Rests on an assumption: The three scenarios (no change, improvement, decrease in β-cell function) exhaustively characterize possible changes in the insulin secretion-sensitivity relationship.
In the paper
“production of insulin is dependent on the proteolytic processing in the -cell secretory granule of proinsulin to insulin and C-peptide (35).”
§ Role of Insulin Secretion and Sensitivity in the Evolution of Type 2 Diabetes in the Diabetes Prevention Program Effects of Lifestyle Intervention and Metformin The Diabetes Prevention Program Research Group* > DISCUSSION
What the sources say
- Not checked — no full text of the sourcecites [35] Duckworth WC, Kitabchi AE, Heinemann M: Direct measurement of plasma proinsulin in normal and diabetic subjects. Am J Med 53:418–427,1972 source
plaindirect- Asserted: passes — The authors put it forward as true.
- Checkable: passes — It can be checked against evidence.
- Load-bearing: fails — The paper’s conclusions may not depend on it.
- Based: passes — The paper gives a reason why it holds.
Probably not a substantial claim. The paper’s conclusions may not depend on it.
The authors state this as an assumption.
Hazard ratios were constant over time.
“Hazard ratios were assumed to be constant over time.”
The paper relies on this without support.
Deterioration of either insulin sensitivity or insulin secretion is critical in determining the progression of hyperglycemia.
“Although the relative importance of decreased insulin sensitivity and insulin secretion in the pathogenesis of type 2 diabetes has been debated, it is generally accepted that deterioration of either or both is critical in determining the progression of hyperglycemia.”
The paper relies on this without support.
Insulin resistance and β-cell dysfunction are central characteristics of type 2 diabetes, impaired fasting glycemia, and impaired glucose tolerance.
“Insulin resistance and -cell dysfunction are two well-established characteristics of type 2 diabetes, impaired fasting glycemia, and impaired glucose tolerance (IGT).”
The paper relies on this without support.
The baseline relationship between insulin secretion and insulin sensitivity is the same across treatment groups.
“The curve represents the regression line of the logarithm of estimated insulin secretion as a linear function of the logarithm of estimated insulin sensitivity for all participants at baseline.”
The paper relies on this without support.
The three scenarios (no change, improvement, decrease in β-cell function) exhaustively characterize possible changes in the insulin secretion-sensitivity relationship.
“changes in insulin secretion may reflect one of three scenarios regarding -cell function.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“In the Diabetes Prevention Program (DPP), greater baseline β-cell function and insulin sensitivity contributed independently to the restoration of NGT following lifestyle changes ( 65 , 66 ).”
From β-Cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment (2014) · cites this paper as [65]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Indeed, higher diabetes incidence in all treatment groups was found among individuals with lower measures of insulin secretory response at baseline in the DPP (22).”
From Increased genetic risk for β-cell failure is associated with β-cell function decline in people with prediabetes (2024) · cites this paper as [22]
In the citing paper
“Successful lifestyle interventions seem to improve insulin sensitivity and β-cell function.92,93”
From Prediabetes: a high-risk state for diabetes development (2012) · cites this paper as [93]
In the citing paper
“Since insulin resistance could increase the risk of AD through both cerebrovascular and Aβ related mechanisms [23]”
From Metformin in Amnestic Mild Cognitive Impairment: Results of a Pilot Randomized Placebo Controlled Clinical Trial (2016) · cites this paper as [23]
In the citing paper
“Large intervention studies with lifestyle interventions and drugs like metformin have shown that it is feasible to decrease hyperinsulinemia and the risk of diabetes (The Diabetes Prevention Program Research, 2005) and is possible that these interventions could extend to decreasing the risk of Alzheimer’s disease.”
From Adiposity, hyperinsulinemia, diabetes and Alzheimer's disease (2008) · cites this paper as The Diabetes Prevention Program Research, 2005
In the citing paper
“Studies showing that metformin (MET) not only reduces insulin levels (11), inflammation and thrombosis (12), and the risk of the metabolic syndrome (13), but also improves insulin sensitivity (11) suggests its potential to exert protective effects on cognitive function.”
From Type 2 Diabetes and Antidiabetic Medications in Relation to Dementia Diagnosis (2014) · cites this paper as [11]
In the citing paper
“The putative mechanisms of MET's positive effects include (i) reducing insulin levels and improving insulin sensitivity (11), (ii) reducing inflammation (11), and (iii) reducing the risk of metabolic syndrome (25).”
From Type 2 Diabetes and Antidiabetic Medications in Relation to Dementia Diagnosis (2014) · cites this paper as [11]
Citations
Cites
Regression Models and Life-Tables
Cox, D. R. (1972) · Journal of the Royal Statistical Society Series B: Statistical Methodology · doi:10.1111/j.2517-6161.1972.tb00899.x · Cited by 39,793
Matthews, D. R., Hosker, J. P., Rudenski, A. S., Naylor, B. A., Treacher, D. F., & Turner, R. C. (1985) · Diabetologia · doi:10.1007/bf00280883 · Cited by 31,502
Toprak, Ö., Kurt, H., Sarı, Y., Şarkış, C., Us, H., & Kırık, A. (2017) · Kidney & Blood Pressure Research · doi:10.1159/000468530 · Cited by 29,772
Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin
(2002) · New England Journal of Medicine · doi:10.1056/nejmoa012512 · Cited by 19,011
Tuomilehto, J., Lindström, J., Eriksson, J. G., Valle, T. T., Hämäläinen, H., Ilanne-Parikka, P., Keinänen-Kiukaanniemi, S., Laakso, M., Louheranta, A., Rastas, M., et al. (2001) · New England Journal of Medicine · doi:10.1056/nejm200105033441801 · Cited by 10,873 · cited 1×
“Finally, the DPP findings are also consistent with a recently reported study that demonstrated that a weight loss intervention in older individuals was associated with improved insulin sensitivity together with a relative preservation of the insulin response reflective of improved β-cell function (31) and provide a pl…”
ResultReport of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus
The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus* (2002) · Diabetes Care · doi:10.2337/diacare.25.2007.s5 · Cited by 10,325
Report of the Expert Committee on the Diagnosis and Classification of Diabetes Mellitus
The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus (1997) · Diabetes Care · doi:10.2337/diacare.20.7.1183 · Cited by 6,220
Pan, X.-R., Li, G.-W., Hu, Y.-H., Wang, J.-X., Yang, W.-Y., An, Z.-X., Hu, Z.-X., Juan-Lin, Xiao, J.-Z., Cao, H.-B., et al. (1997) · Diabetes Care · doi:10.2337/diacare.20.4.537 · Cited by 4,320
The Triumvirate: β-Cell, Muscle, Liver: A Collusion Responsible for NIDDM
DeFronzo, R. A. (1988) · Diabetes · doi:10.2337/diab.37.6.667 · Cited by 2,456
Kahn, S. E., Prigeon, R. L., McCulloch, D. K., Boyko, E. J., Bergman, R. N., Schwartz, M. W., Neifing, J. L., Ward, W. K., Beard, J. C., & Palmer, J. P. (1993) · Diabetes · doi:10.2337/diab.42.11.1663 · Cited by 1,405
Cited by
Sorted by citations
Prediabetes: a high-risk state for diabetes development
Tabák, A. G., Herder, C., Rathmann, W., Brunner, E. J., & Kivimäki, M. (2012) · The Lancet · doi:10.1016/s0140-6736(12)60283-9 · Cited by 2,958
Tabák, A. G., Jokela, M., Akbaraly, T. N., Brunner, E. J., Kivimäki, M., & Witte, D. R. (2009) · The Lancet · doi:10.1016/s0140-6736(09)60619-x · Cited by 898
Morino, K., Petersen, K. F., & Shulman, G. I. (2006) · Diabetes · doi:10.2337/db06-s002 · Cited by 853
TCF7L2 Polymorphisms and Progression to Diabetes in the Diabetes Prevention Program
Florez, J. C., Jablonski, K. A., Bayley, N., Pollin, T. I., de Bakker, P. I. W., Shuldiner, A. R., Knowler, W. C., Nathan, D. M., & Altshuler, D. (2006) · New England Journal of Medicine · doi:10.1056/nejmoa062418 · Cited by 834
Association of an intensive lifestyle intervention with remission of type 2 diabetes
Gregg, E. W., Chen, H., Wagenknecht, L. E., Clark, J. M., Delahanty, L. M., Bantle, J., Pownall, H. J., Johnson, K. C., Safford, M. M., Kitabchi, A. E., et al. (2012) · JAMA · doi:10.1001/jama.2012.67929 · Cited by 752
Abdul-Ghani, M. A., Tripathy, D., & DeFronzo, R. A. (2006) · Diabetes Care · doi:10.2337/dc05-2179 · Cited by 744
Brain Insulin Resistance at the Crossroads of Metabolic and Cognitive Disorders in Humans
Kullmann, S., Heni, M., Hallschmid, M., Fritsche, A., Preissl, H. T., & Häring, H. (2016) · Physiological Reviews · doi:10.1152/physrev.00032.2015 · Cited by 654
Utzschneider, K. M., Prigeon, R. L., Faulenbach, M. V., Tong, J., Carr, D. B., Boyko, E. J., Leonetti, D. L., McNeely, M. J., Fujimoto, W. Y., & Kahn, S. E. (2009) · Diabetes Care · doi:10.2337/dc08-1478 · Cited by 572
Perreault, L., Pan, Q., Mather, K. J., Watson, K. E., Hamman, R. F., & Kahn, S. E. (2012) · The Lancet · doi:10.1016/s0140-6736(12)60525-x · Cited by 532
From pre-diabetes to diabetes: diagnosis, treatments and translational research
Khan, R., Chua, Z., Tan, J., Yang, Y., Liao, Z., & Zhao, Y. (2019) · Medicina · doi:10.3390/medicina55090546 · Cited by 484
“Insulin sensitivity improves 30% by losing only 5% of body weight [151].”
Backgroundβ-Cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment
Halban, P. A., Polonsky, K. S., Bowden, D. W., Hawkins, M. A., Ling, C., Mather, K. J., Powers, A. C., Rhodes, C. J., Sussel, L., & Weir, G. C. (2014) · Diabetes Care · doi:10.2337/dc14-0396 · Cited by 460
Prevention of Type 2 Diabetes by Lifestyle Changes: A Systematic Review and Meta-Analysis
Uusitupa, M. I. J., Khan, T. A., Viguiliouk, E., Kahleová, H., Rivellese, A. A., Hermansen, K., Pfeiffer, A. F. H., Thanopoulou, A. C., Salas‐Salvadó, J., Schwab, U., et al. (2019) · Nutrients · doi:10.3390/nu11112611 · Cited by 531
Wu, R.-R., Zhao, J.-P., Jin, H., Shao, P., Fang, M.-S., Guo, X.-F., He, Y.-Q., Liu, Y.-J., Chen, J.-D., & Li, L.-H. (2008) · JAMA · doi:10.1001/jama.2007.56-b · Cited by 366
Hyperbolic Relationship Between Insulin Secretion and Sensitivity on Oral Glucose Tolerance Test
Retnakaran, R. R., Shen, S., Hanley, A. J., Vuksan, V. V. V., Hamilton, J. K., & Zinman, B. (2008) · Obesity · doi:10.1038/oby.2008.307 · Cited by 367
Salsalate Improves Glycemia and Inflammatory Parameters in Obese Young Adults
Fleischman, A., Shoelson, S. E., Bernier, R., & Goldfine, A. B. (2008) · Diabetes Care · doi:10.2337/dc07-1338 · Cited by 346
Nyenwe, E. A., Jerkins, T. W., Umpierrez, G. E., & Kitabchi, A. E. (2010) · Metabolism · doi:10.1016/j.metabol.2010.09.010 · Cited by 355
Evaluation of proposed oral disposition index measures in relation to the actual disposition index
Retnakaran, R. R., Qi, Y., Goran, M. I., & Hamilton, J. K. (2009) · Diabetic Medicine · doi:10.1111/j.1464-5491.2009.02841.x · Cited by 324
DeFronzo, R. A., & Abdul‐Ghani, M. A. (2011) · The American Journal of Cardiology · doi:10.1016/j.amjcard.2011.03.013 · Cited by 324
Jean‐Louis, G., Zizi, F., Clark, L. T., Brown, C. D., & McFarlane, S. I. (2008) · Journal of Clinical Sleep Medicine · doi:10.5664/jcsm.27191 · Cited by 313
Satoh, H., Ohira, T., Hosoya, M., Sakai, A., Watanabe, T., Ohtsuru, A., Kawasaki, Y., Suzuki, H., Takahashi, A., Kobashi, G., et al. (2015) · Journal of Diabetes Research · doi:10.1155/2015/415253 · Cited by 301
Molecular and cellular mechanisms linking inflammation to insulin resistance and β-cell dysfunction
Khodabandehloo, H., Gorgani‐Firuzjaee, S., Panahi, G., & Meshkani, R. (2015) · Translational research · doi:10.1016/j.trsl.2015.08.011 · Cited by 307
Link between type 2 diabetes and Alzheimer’s disease: from epidemiology to mechanism and treatment
Li, X., Leng, S. X., & Song, D. (2015) · Clinical Interventions in Aging · doi:10.2147/cia.s74042 · Cited by 314
Prediabetes and Cardiovascular Disease
Brannick, B., & Dagogo-Jack, S. (2018) · Endocrinology and Metabolism Clinics of North America · doi:10.1016/j.ecl.2017.10.001 · Cited by 293
Hydroxychloroquine and Risk of Diabetes in Patients With Rheumatoid Arthritis
Wasko, M. C., Hubert, H. B., Lingala, B., Elliott, J. R., Luggen, M. E., Fries, J. F., & Ward, M. M. (2007) · JAMA · doi:10.1001/jama.298.2.187 · Cited by 293
Bensellam, M., Laybutt, D. R., & Jonas, J. (2012) · Molecular and Cellular Endocrinology · doi:10.1016/j.mce.2012.08.003 · Cited by 304
“…of -cell function despite intensive therapy (Turner, 1998; UKPDS, 1998) individuals through enhancement of insulin sensitivity and -cell function (Kitabchi et al., 2005; Knowler et al., 2002) Diazoxide and other KATP channel openers - Opening of the KATP channel and inhibition of insulin…”
BackgroundLuchsinger, J. A., Perez, T., Chang, H., Mehta, P., Steffener, J., Pradabhan, G., Ichise, M., Manly, J., Devanand, D. P., & Bagiella, E. (2016) · Journal of Alzheimer's Disease · doi:10.3233/jad-150493 · Cited by 285
Therapeutic Use of Metformin in Prediabetes and Diabetes Prevention
Gottwald‐Hostalek, U., Gwilt, M., & Hildemann, S. K. (2015) · Drugs · doi:10.1007/s40265-015-0416-8 · Cited by 283
The prevention of type 2 diabetes
F. T. D. P. P. R. G., Crandall, J. P., Knowler, W. C., Kahn, S. E., Marrero, D., Florez, J. C., Bray, G. A., Haffner, S. M., Hoskin, M., & Nathan, D. M. (2008) · Nature Clinical Practice Endocrinology & Metabolism · doi:10.1038/ncpendmet0843 · Cited by 261
The Diabetes Prevention Program Research Group [Prepared by Jill Crandall, D. S. (2006) · The Journals of Gerontology Series A: Biological Sciences and Medical Sciences · doi:10.1093/gerona/61.10.1075 · Cited by 254
Glucose Intolerance in Pregnancy and Future Risk of Pre-Diabetes or Diabetes
Retnakaran, R. R., Qi, Y., Sermer, M., Connelly, P. W., Hanley, A. J., & Zinman, B. (2008) · Diabetes Care · doi:10.2337/dc08-0972 · Cited by 251
Preservation of β-Cell Function: The Key to Diabetes Prevention
DeFronzo, R. A., & Abdul-Ghani, M. A. (2011) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2011-0246 · Cited by 247
Kahn, S. E., Lachin, J. M., Zinman, B., Haffner, S. M., Aftring, R. P., Paul, G., Kravitz, B. G., Herman, W. H., Viberti, G., Holman, R. R., et al. (2011) · Diabetes · doi:10.2337/db10-1392 · Cited by 249
Schrieks, I. C., Heil, A. L. J., Hendriks, H. F. J., Mukamal, K. J., & Beulens, J. W. J. (2015) · Diabetes Care · doi:10.2337/dc14-1556 · Cited by 238
Incretin-Based Therapies in Type 2 Diabetes Mellitus
Chia, C. W., & Egan, J. M. (2008) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2007-2109 · Cited by 223
β-Cell Failure in Type 2 Diabetes: Postulated Mechanisms and Prospects for Prevention and Treatment
Halban, P. A., Polonsky, K. S., Bowden, D. W., Hawkins, M. A., Ling, C., Mather, K. J., Powers, A. C., Rhodes, C. J., Sussel, L., & Weir, G. C. (2014) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2014-1425 · Cited by 242
Insulin resistance and impaired beta cell function in rheumatoid arthritis
Dessein, P. H., & Joffe, B. I. (2006) · Arthritis & Rheumatism · doi:10.1002/art.22053 · Cited by 218
Adiposity, Type 2 Diabetes, and Alzheimer's Disease
Luchsinger, J. A., & Gustafson, D. (2009) · Journal of Alzheimer s Disease · doi:10.3233/jad-2009-1022 · Cited by 221
Type 2 Diabetes and Cognitive Impairment: Linking Mechanisms
Luchsinger, J. A. (2012) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-111433 · Cited by 205
Aroda, V. R., Knowler, W. C., Crandall, J. P., Perreault, L., Edelstein, S. L., Jeffries, S., Molitch, M. E., Pi-Sunyer, X., Darwin, C. H., Heckman‐Stoddard, B. M., et al. (2017) · Diabetologia · doi:10.1007/s00125-017-4361-9 · Cited by 203
“Effects of metformin on diabetes prevention In 2002, the DPP published its primary findings from the masked-treatment phase, showing that the ILS and metformin groups had a respective 58% and 31% lower incidence of diabetes than the placebo group [2].”
BackgroundInfluentialKnowler (2011) · doi:10.1001/archinternmed.2011.367 · Cited by 194
Esser, N., Utzschneider, K. M., & Kahn, S. E. (2020) · Diabetologia · doi:10.1007/s00125-020-05245-x · Cited by 212
Protein intake and ovulatory infertility
Chavarro, J. E., Rich-Edwards, J. W., ROSNER, B. A., & Willett, W. C. (2008) · American Journal of Obstetrics and Gynecology · doi:10.1016/j.ajog.2007.06.057 · Cited by 187
Chavarro, J. E., Rich-Edwards, J. W., ROSNER, B. A., & Willett, W. C. (2007) · European Journal of Clinical Nutrition · doi:10.1038/sj.ejcn.1602904 · Cited by 181
Wang, J., Kuusisto, J., Vänttinen, M., Kuulasmaa, T., Lindström, J., Tuomilehto, J. O., Uusitupa, M. I. J., & Laakso, M. (2007) · Diabetologia · doi:10.1007/s00125-007-0656-6 · Cited by 180
Brannick, B., Wynn, A., & Dagogo-Jack, S. E. (2016) · Experimental Biology and Medicine · doi:10.1177/1535370216654227 · Cited by 189
The RISE Consortium, Nadeau, K. J., Hannon, T. S., Edelstein, S. L., Arslanian, S. A., Caprio, S., Leschek, E. W., Zeitler, P. S., Buchanan, T. A., Ehrmann, D. A., et al. (2018) · Diabetes Care · doi:10.2337/dc18-0787 · Cited by 176
Cnop, M., Vidal, J., Hull, R. L., Utzschneider, K. M., Carr, D. B., Schraw, T., Scherer, P. E., Boyko, E. J., Fujimoto, W. Y., & Kahn, S. E. (2007) · Diabetes Care · doi:10.2337/dc06-1834 · Cited by 174
Adiposity, hyperinsulinemia, diabetes and Alzheimer's disease
Luchsinger, J. A. (2008) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2008.02.048 · Cited by 171
Gestational Diabetes After Delivery
Kitzmiller, J. L., Dang-Kilduff, L., & Taslimi, M. M. (2007) · Diabetes Care · doi:10.2337/dc07-s221 · Cited by 179
TCF7L2 Polymorphisms Modulate Proinsulin Levels and β-Cell Function in a British Europid Population
Loos, R. J. F., Franks, P. W., Francis, R. W., Barroso, I., Gribble, F. M., Savage, D. B., Ong, K. K., O’Rahilly, S., & Wareham, N. J. (2007) · Diabetes · doi:10.2337/db07-0055 · Cited by 169
Adiposity and Alzheimer's disease
Luchsinger, J. A., & Gustafson, D. (2008) · Current Opinion in Clinical Nutrition & Metabolic Care · doi:10.1097/mco.0b013e32831c8c71 · Cited by 181
Type 2 Diabetes and Antidiabetic Medications in Relation to Dementia Diagnosis
Cheng, C., Lin, C.-H., Tsai, Y.-W., Tsai, C.-J., Chou, P.-H., & Lan, T.-H. (2014) · The Journals of Gerontology: Series A · doi:10.1093/gerona/glu073 · Cited by 167
Adiponectin, Change in Adiponectin, and Progression to Diabetes in the Diabetes Prevention Program
Mather, K. J., Funahashi, T., Matsuzawa, Y., Edelstein, S. L., Bray, G. A., Kahn, S. E., Crandall, J. P., Marcovina, S. M., Goldstein, B., Goldberg, R. B., et al. (2008) · Diabetes · doi:10.2337/db07-1419 · Cited by 161
“Insulin sensitivity was assessed using inverse fasting insulin levels, as in our prior publications (28).”
MethodAdherence to Preventive Medications
Walker, E. A., Molitch, M., Kramer, M. K., Kahn, S., Ma, Y., Edelstein, S., Smith, K., Johnson, M. K., Kitabchi, A., Crandall, J., et al. (2006) · Diabetes Care · doi:10.2337/dc06-0454 · Cited by 161
Cárdenas, A., Gold, D. R., Hauser, R. B., Kleinman, K., Hivert, M., Calafat, A. M., Ye, X., Webster, T. F., Horton, E. S., & Oken, E. (2017) · Environmental Health Perspectives · doi:10.1289/ehp1612 · Cited by 145
“As previously demonstrated in the DPP, the e ff ect of the life-style intervention was strongly associated with diabetes incidence and had a large in fl uence on metabolic and glycemic markers over time (Kitabchi et al. 2005).”
Statin use and risk of developing diabetes: results from the Diabetes Prevention Program
Crandall, J. P., Mather, K., Rajpathak, S. N., Goldberg, R. B., Watson, K., Foo, S., Ratner, R., Barrett-Connor, E., & Temprosa, M. (2017) · BMJ Open Diabetes Research & Care · doi:10.1136/bmjdrc-2017-000438 · Cited by 137
Cefalu, W. T., Buse, J. B., Tuomilehto, J. O., Fleming, G. A., Ferrannini, E., Gerstein, H. C., Bennett, P. H., Ramachandran, A., Raz, I., Rosenstock, J., et al. (2016) · Diabetes Care · doi:10.2337/dc16-0873 · Cited by 148
Gong, X., Ji, M., Xu, J., Zhang, C., & Li, M. (2019) · Critical Reviews in Food Science and Nutrition · doi:10.1080/10408398.2019.1634517 · Cited by 146
Diabetes Prevention Program Research Group (2015) · Diabetes Care · doi:10.2337/dc14-0886 · Cited by 139
Florez, J. C., Jablonski, K. A., Sun, M. W., Bayley, N., Kahn, S. E., Shamoon, H., Hamman, R. F., Knowler, W. C., Nathan, D. M., & Altshuler, D. (2007) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2006-2275 · Cited by 131
Yoon, U., Kwok, L. L., & Magkidis, A. (2012) · Metabolism · doi:10.1016/j.metabol.2012.07.009 · Cited by 132
Detweiler-Bedell, J. B., Friedman, M. A., Leventhal, H., Miller, I. W., & Leventhal, E. A. (2008) · Clinical Psychology Review · doi:10.1016/j.cpr.2008.09.002 · Cited by 128
Florez, J. C., Jablonski, K. A., Kahn, S. E., Franks, P. W., Dabelea, D., Hamman, R. F., Knowler, W. C., Nathan, D. M., & Altshuler, D. (2007) · Diabetes · doi:10.2337/db06-0966 · Cited by 119
Inflammation and schizophrenia
Fan, X., GOFF, D. C., & Henderson, D. C. (2007) · Expert Review of Neurotherapeutics · doi:10.1586/14737175.7.7.789 · Cited by 121
Body Size and Shape Changes and the Risk of Diabetes in the Diabetes Prevention Program
Fujimoto, W. Y., Jablonski, K. A., Bray, G. A., Kriska, A. M., Barrett-Connor, E. L., Haffner, S. M., Hanson, R. L., Hill, J. O., Hubbard, V. S., Stamm, E. R., et al. (2007) · Diabetes · doi:10.2337/db07-0009 · Cited by 117
Fowler, S. P. (2016) · Physiology & Behavior · doi:10.1016/j.physbeh.2016.04.047 · Cited by 117
Ehrmann, D. A., Temple, K. A., Rue, A., Barengolts, E., Mokhlesi, B., Cauter, E. V., Sam, S., Miller, M. A., Kahn, S. E., Atkinson, K. M., et al. (2018) · Diabetes Care · doi:10.2337/dc18-0243 · Cited by 121
Lorenzo, C., Wagenknecht, L. E., Agostino, R. B. D., Rewers, M., Karter, A. J., & Haffner, S. M. (2009) · Diabetes Care · doi:10.2337/dc09-1115 · Cited by 117
Anti-Diabetic Effect of Portulaca oleracea L. Polysaccharideandits Mechanism in Diabetic Rats
Bai, Y., Zang, X., Ma, J., & Xu, G. (2016) · International Journal of Molecular Sciences · doi:10.3390/ijms17081201 · Cited by 109
Lachin, J. M., Christophi, C. A., Edelstein, S. L., Ehrmann, D. A., Hamman, R. F., Kahn, S. E., Knowler, W. C., Nathan, D. M., & on behalf of the DPP Research Group (2007) · Diabetes · doi:10.2337/db06-0918 · Cited by 107
Prevention of Diabetes With Pioglitazone in ACT NOW
DeFronzo, R. A., Tripathy, D., Schwenke, D. C., Banerji, M., Bray, G. A., Buchanan, T. A., Clement, S. C., Gastaldelli, A., Henry, R. R., Kitabchi, A. E., et al. (2013) · Diabetes · doi:10.2337/db13-0265 · Cited by 109
Metformin, beyond an insulin sensitizer, targeting heart and pancreatic β cells
Yang, X., Xu, Z., Zhang, C., Cai, Z., & Zhang, J. (2016) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.09.019 · Cited by 108
Bloem, C. J., & Chang, A. M. (2007) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2007-1734 · Cited by 107
A preclinical overview of metformin for the treatment of type 2 diabetes
Zhou, T., Xu, X., Du, M., Zhao, T., & Wang, J. (2018) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2018.07.085 · Cited by 107
A cross-sectional study of vitamin D and insulin resistance in children
Kelly, A. T., Brooks, L. J., Dougherty, S., Carlow, D. C., & Zemel, B. S. (2011) · Archives of Disease in Childhood · doi:10.1136/adc.2010.187591 · Cited by 100
Fritsche, A., Wagner, R. J., Heni, M., Kantartzis, K., Machann, J., Schick, F., Lehmann, R., Peter, A., Dannecker, C., Fritsche, L., et al. (2021) · Diabetes · doi:10.2337/db21-0526 · Cited by 104
The RISE Consortium (2013) · Diabetes Care · doi:10.2337/dc13-1879 · Cited by 101
Lifestyle intervention for prevention of diabetes: determinants of success for future implementation
Roumen, C., Blaak, E. E., & Corpeleijn, E. (2009) · Nutrition Reviews · doi:10.1111/j.1753-4887.2009.00181.x · Cited by 96
Goldberg, R. B., Temprosa, M. G., Haffner, S. M., Orchard, T. J., Ratner, R. E., Fowler, S. E., Mather, K. J., Marcovina, S. M., Saudek, C. D., Matulik, M. J., et al. (2009) · Diabetes Care · doi:10.2337/dc08-0494 · Cited by 91
Retnakaran, R. R., Qi, Y., Sermer, M., Connelly, P. W., Zinman, B., & Hanley, A. J. (2008) · Diabetes Care · doi:10.2337/dc08-0126 · Cited by 88
“In pregnant women, ISOGTT exhibits better correlation with insulin sensitivity measured by euglycemic-hyperinsulinemic clamp than either homeostasis model assessment of insulin resistance (HOMA-IR) or quantitative insulin sensitivity check in- dex (12).”
MethodInfluentialSatoh, H., Ohira, T., Hosoya, M., Sakai, A., Watanabe, T., Ohtsuru, A., Kawasaki, Y., Suzuki, H., Takahashi, A., Kobashi, G., et al. (2015) · Journal of Diabetes Research · doi:10.1155/2015/627390 · Cited by 91
“Intensive lifestyle interventionwas more effective than medication in slowing the progression to diabetes, partially due to the fact that lifestyle modifications provide greater improvements in insulin sensitivity andβ-cell functions [9].”
Hanley, A. J., Retnakaran, R. R., Qi, Y., Gerstein, H. C., Perkins, B. A., Raboud, J., Harris, S. B., & Zinman, B. (2009) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2009-0719 · Cited by 90
Endothelial dysfunction, ADMA and insulin resistance in essential hypertension
Perticone, F., Sciacqua, A., Maio, R., Perticone, M., Leone, G. G., Bruni, R., Cello, S. D., Pascale, A., Talarico, G., Greco, L., et al. (2009) · International Journal of Cardiology · doi:10.1016/j.ijcard.2008.12.131 · Cited by 88
Diabetes, related conditions, and dementia
Luchsinger, J. A. (2010) · Journal of the Neurological Sciences · doi:10.1016/j.jns.2010.08.063 · Cited by 88
Hofsø, D., Jenssen, T. G., Bollerslev, J., Ueland, T., Godang, K., Stümvoll, M., Sandbu, R., Røislien, J., & Hjelmesaeth, J. S. (2010) · European Journal of Endocrinology · doi:10.1530/eje-10-0804 · Cited by 83
Deciphering the Roles of Metformin in Alzheimer’s Disease: A Snapshot
Liao, W., Xu, J., Li, B., Ruan, Y., Li, T., & Liu, J. (2022) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.728315 · Cited by 84
Kanat, M., DeFronzo, R. A., & Abdul‐Ghani, M. A. (2015) · World Journal of Diabetes · doi:10.4239/wjd.v6.i12.1207 · Cited by 87
Can New-Onset Diabetes After Kidney Transplant Be Prevented?
Chakkera, H. A., Weil, E. J., Pham, P. T., Pomeroy, J. J., & Knowler, W. C. (2013) · Diabetes Care · doi:10.2337/dc12-2067 · Cited by 80
Metformin for treatment of antipsychotic-induced weight gain: A randomized, placebo-controlled study
Wang, M., Tong, J.-H., Zhu, G., Liang, G.-M., Yan, H., & Wang, X. (2012) · Schizophrenia Research · doi:10.1016/j.schres.2012.02.021 · Cited by 80
Fan, X., Liu, E. Y., Freudenreich, O., Park, J. H., Liu, D., Wang, J., Yi, Z., GOFF, D. C., & Henderson, D. C. (2010) · Schizophrenia Research · doi:10.1016/j.schres.2010.02.1028 · Cited by 78
“A variety of data indicate that insulin resistance plays a central role in the development of diabetes and other metabolic disturbances (Kitabchi et al., 2005; Semenkovich, 2006).”
BackgroundExercise and diabetes: relevance and causes for response variability
Böhm, A., Weigert, C., Staiger, H., & Häring, H. (2015) · Endocrine · doi:10.1007/s12020-015-0792-6 · Cited by 83
ß‐cell function and anti‐diabetic pharmacotherapy
Prato, S. D., Bianchi, C., & Marchetti, P. (2007) · Diabetes/Metabolism Research and Reviews · doi:10.1002/dmrr.770 · Cited by 79
The Effects of Metformin and Weight Loss on Biomarkers Associated With Breast Cancer Outcomes
Patterson, R. E., Marinac, C. R., Sears, D. D., Kerr, J., Hartman, S. J., Cadmus‐Bertram, L., Villaseñor, A., Flatt, S. W., Godbole, S. V., Li, H., et al. (2018) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/djy040 · Cited by 77
Gradmark, A., Pomeroy, J. J., Renström, F., Steiginga, S., Persson, M., Wright, A., Bluck, L. J. C., Domellöf, M., Kahn, S. E., Mogren, I., et al. (2011) · BMC Pregnancy and Childbirth · doi:10.1186/1471-2393-11-44 · Cited by 78
Burns, S. F., Bacha, F. F., Lee, S., Tfayli, H. M., Gungor, N., & Arslanian, S. A. (2011) · Diabetes Care · doi:10.2337/dc11-0423 · Cited by 75
“Recently, a nonlinear function describing the relationship between the oral glucose–induced early insulin response and insulin sensitivity has been used to assess b-cell function in both observational (18) and interventional studies in adults (19).”
Metformin, lifestyle intervention, and cognition in the Diabetes Prevention Program Outcomes Study
Luchsinger, J. A., Ma, Y., Christophi, C. A., Florez, H., Golden, S. H., Hazuda, H., Crandall, J., Venditti, E., Watson, K., Jeffries, S., et al. (2017) · Diabetes Care · doi:10.2337/dc16-2376 · Cited by 75
Serván, P. R. (2013) · PubMed · doi:10.3305/nh.2013.28.sup5.6929 · Cited by 81
“Improvements in insulin sensitivity and insulin secretion, greatest in the intensive lifestyle intervention group, and somewhat lower in the metformin group, correlated directly with decreased risk of diabetes.(18) Lifestyle intervention may also be effective in individuals without impaired glucose tolerance in the MR…”
BackgroundPorter, K. M., Ward, M., Hughes, C., O’Kane, M., Hoey, L., McCann, A., Molloy, A. M., Cunningham, C. J., Casey, M. C., Tracey, F., et al. (2019) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2018-01791 · Cited by 75
The RISE Consortium, Ehrmann, D. A., Temple, K. A., Rue, A., Barengolts, E., Mokhlesi, B., Van Cauter, E., Sam, S., Miller, M. A., Kahn, S. E., et al. (2019) · Diabetes Care · doi:10.2337/dc19-0556 · Cited by 73
Metadata
- Authors
- The Diabetes Prevention Program Research Group
- Affiliations
- George Washington University (US)
- Corresponding author
- The Diabetes Prevention Program Research Group
- Venue
- Diabetes
- Publisher
- American Diabetes Association
- Published
- 2005-08-01
- Volume
- 54
- Issue
- 8
- Pages
- 2404-2414
- ISSN
- 0012-1797 (ISSN-L)
- 1939-327X
- PMC
- PMC1360738
- OpenAlex
- W11872906
- Semantic Scholar
- 325f16dd65ffe228accc202bdf7b70e715176447
- Cited by
- 446
- References
- 49
- Citations by year
- 2026: 12 · 2025: 9 · 2024: 16 · 2023: 19 · 2022: 14 · 2021: 19 · 2020: 19 · 2019: 18 · 2018: 22 · 2017: 17 · 2016: 26 · 2015: 24 · 2014: 26 · 2013: 17 · 2012: 31
- FWCI
- 16.99
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Diabetes (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- American Diabetes Association
- Bristol-Myers Squibb
- National Institutes of Health
- Centers for Disease Control and Prevention
- National Institute on Aging
- National Institute of Diabetes and Digestive and Kidney Diseases (U01DK048489)
- National Institute of Child Health and Human Development
- National Center for Research Resources
- Office of Women's Health
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes, Cardiovascular Risks, and Lipoproteins
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Pancreatic function and diabetes
- Keywords
- type 2 diabetes prevention, insulin secretion, insulin sensitivity, insulin resistance, beta-cell dysfunction, impaired glucose tolerance, metformin, intensive lifestyle intervention, Diabetes Prevention Program, diabetes incidence, weight change
- MeSH terms
- Insulin Secretion, Adult, Blood Glucose, Body Weight, Diabetes Mellitus, Type 2, Fasting, Female, Glucose Tolerance Test, Humans, Hypoglycemic Agents, Insulin, Insulin Resistance, Islets of Langerhans, Life Style, Male, Metformin, Middle Aged, Placebos
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-10-11, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-10-11 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review